Abstract
A substantial proportion of genes that control fetal growth in placental mammals are imprinted. Imprinted genes can act in fetal tissues to regulate growth by cell proliferation, cell death and the make up of extracellular space. Imprinted growth-promoting genes such as Igf2 probably act predominantly in an endocrine fashion, thus coordinating organ growth with the growth of the organism. In overgrowth and growth deficiency syndromes, however, imprinted growth factors can act by more local mechanisms, resulting in disproportionate growth. In addition to controlling fetal growth directly and thereby determining the nutritional demand of the fetus, imprinted genes can also apparently limit the nutritional supply to the fetus through the placenta. Imprinted genes may also be involved in postnatal growth up to weaning.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Animals
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Cell Cycle / physiology
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Cell Size
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DNA / metabolism
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Embryonic and Fetal Development*
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Genes
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Genomic Imprinting*
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Humans
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Insulin / genetics
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Insulin / metabolism
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Insulin-Like Growth Factor I / genetics
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Insulin-Like Growth Factor I / metabolism
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Insulin-Like Growth Factor II / genetics
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Insulin-Like Growth Factor II / metabolism
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Mammals / embryology
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Mammals / genetics*
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Mammals / growth & development*
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Mammals / physiology
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Placenta / physiology
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Receptor, IGF Type 1 / genetics
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Receptor, IGF Type 1 / metabolism
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Receptor, IGF Type 2 / genetics
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Receptor, IGF Type 2 / metabolism
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Receptor, Insulin / genetics
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Receptor, Insulin / metabolism
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Signal Transduction / physiology
Substances
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Insulin
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Receptor, IGF Type 2
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Insulin-Like Growth Factor I
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Insulin-Like Growth Factor II
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DNA
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Receptor, IGF Type 1
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Receptor, Insulin